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BCG-induced enhancement of endotoxin sensitivity in C3H/HeJ mice. II. T cell modulation of macrophage sensitivity to LPS in vitro.

作者信息

Vogel S N, Weedon L L, Wahl L M, Rosenstreich D L

出版信息

Immunobiology. 1982 Feb;160(5):479-93. doi: 10.1016/S0171-2985(82)80010-7.

DOI:10.1016/S0171-2985(82)80010-7
PMID:6802744
Abstract
摘要

相似文献

1
BCG-induced enhancement of endotoxin sensitivity in C3H/HeJ mice. II. T cell modulation of macrophage sensitivity to LPS in vitro.卡介苗诱导C3H/HeJ小鼠内毒素敏感性增强。II. 体外T细胞对巨噬细胞LPS敏感性的调节
Immunobiology. 1982 Feb;160(5):479-93. doi: 10.1016/S0171-2985(82)80010-7.
2
BCG-induced enhancement of endotoxin sensitivity in C3H/HeJ mice. I. In vivo studies.卡介苗诱导C3H/HeJ小鼠内毒素敏感性增强。I. 体内研究。
J Immunol. 1980 Apr;124(4):2004-9.
3
Induction of nitrite/nitrate synthesis in murine macrophages by BCG infection, lymphokines, or interferon-gamma.卡介苗感染、淋巴因子或γ干扰素诱导小鼠巨噬细胞中亚硝酸盐/硝酸盐的合成。
J Immunol. 1987 Jul 15;139(2):518-25.
4
Macrophage stimulation by bacterial lipopolysaccharides. III. Selective unresponsiveness of C3H/HeJ macrophages to the lipid A differentiation signal.细菌脂多糖对巨噬细胞的刺激作用。III. C3H/HeJ巨噬细胞对脂质A分化信号的选择性无反应性。
J Immunol. 1979 Nov;123(5):2304-10.
5
Endotoxin-induced interferon-gamma production in culture cells derived from BCG-infected C3H/HeJ mice.内毒素诱导卡介苗感染的C3H/HeJ小鼠来源培养细胞产生γ干扰素
J Immunol. 1988 Jan 15;140(2):494-500.
6
Macrophage sensitivity to endotoxin: genetic control by a single codominant gene.巨噬细胞对内毒素的敏感性:由单个共显性基因进行遗传控制。
J Immunol. 1978 Nov;121(5):1664-70.
7
The activation of tumoricidal properties in macrophages of endotoxin responder and nonresponder mice by liposome-encapsulated immunomodulators.脂质体包裹的免疫调节剂对内毒素反应小鼠和无反应小鼠巨噬细胞杀肿瘤特性的激活作用。
J Reticuloendothel Soc. 1983 Mar;33(3):165-74.
8
Modulation of macrophage Ia-expression by lipopolysaccharide. I. Induction of Ia expression in vivo.脂多糖对巨噬细胞Ia表达的调节。I. 体内Ia表达的诱导
J Immunol. 1984 Oct;133(4):1825-35.
9
Defective tumoricidal capacity of macrophages from P/J mice: characterization of the macrophage cytotoxic defect after in vivo and in vitro activation stimuli.P/J 小鼠巨噬细胞的肿瘤杀伤能力缺陷:体内和体外激活刺激后巨噬细胞细胞毒性缺陷的特征
J Immunol. 1980 Aug;125(2):771-6.
10
Macrophage-T cell interaction in experimental mycobacterial infection. Selective regulation of co-stimulatory molecules on Mycobacterium-infected macrophages and its implication in the suppression of cell-mediated immune response.实验性分枝杆菌感染中的巨噬细胞- T细胞相互作用。分枝杆菌感染的巨噬细胞上共刺激分子的选择性调节及其在抑制细胞介导免疫反应中的意义。
Eur J Immunol. 1994 Nov;24(11):2618-24. doi: 10.1002/eji.1830241108.

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Nasal immunization with Porphyromonas gingivalis outer membrane protein decreases P. gingivalis-induced atherosclerosis and inflammation in spontaneously hyperlipidemic mice.用牙龈卟啉单胞菌外膜蛋白进行鼻腔免疫可减轻牙龈卟啉单胞菌诱导的自发性高脂血症小鼠的动脉粥样硬化和炎症。
Infect Immun. 2008 Jul;76(7):2958-65. doi: 10.1128/IAI.01572-07. Epub 2008 Apr 21.
2
Bacterial induction of beta interferon in mice is a function of the lipopolysaccharide component.细菌在小鼠体内诱导β干扰素是脂多糖成分的一种功能。
Infect Immun. 2000 Mar;68(3):1600-7. doi: 10.1128/IAI.68.3.1600-1607.2000.
3
Induction of hyperreactivity to endotoxin in mice by Coxiella burnetii.
伯纳特柯克斯体诱导小鼠对内毒素产生高反应性
Infect Immun. 1984 Sep;45(3):713-7. doi: 10.1128/iai.45.3.713-717.1984.
4
Silica enhancement of murine endotoxin sensitivity.二氧化硅增强小鼠对内毒素的敏感性。
Infect Immun. 1982 Nov;38(2):681-5. doi: 10.1128/iai.38.2.681-685.1982.
5
Requirement for lipopolysaccharide-responsive macrophages in galactosamine-induced sensitization to endotoxin.半乳糖胺诱导的内毒素致敏中对脂多糖反应性巨噬细胞的需求。
Infect Immun. 1986 Mar;51(3):891-5. doi: 10.1128/iai.51.3.891-895.1986.
6
Mammalian nitrate biosynthesis: mouse macrophages produce nitrite and nitrate in response to Escherichia coli lipopolysaccharide.哺乳动物硝酸盐生物合成:小鼠巨噬细胞在响应大肠杆菌脂多糖时产生亚硝酸盐和硝酸盐。
Proc Natl Acad Sci U S A. 1985 Nov;82(22):7738-42. doi: 10.1073/pnas.82.22.7738.
7
The role of macrophages in LPS-induced lethality and tissue injury.巨噬细胞在脂多糖诱导的致死率和组织损伤中的作用。
Immunology. 1988 Mar;63(3):521-7.
8
Endotoxin-induced uveitis in the rat. A study of the role of inflammation mediators.大鼠内毒素诱导性葡萄膜炎。炎症介质作用的研究。
Graefes Arch Clin Exp Ophthalmol. 1988;226(6):553-8. doi: 10.1007/BF02169204.